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PubMedDate not supplied

Polymorphism of C3 components and the B factor in patients with chronic renal failure, dialyzed iteratively.

The value of C3, of the cleavage C3 components and of the B factor were determined in 25 normal controls and in 22 patients with chronic renal failure (CRF), iteratively dialyzed. Low values of C3 and progressive hypomorphism of the cleavage components of C3 were observed in the patients at the three moments of determination. The activity of the B factor was also found significantly decreased in the patients. Our results indicated an activation of the complement alternative pathway in the dialyzed patients but the activation through the classic pathway, could not be excluded either. It is concluded that this activation might be due to the initial disease which generated CRF but also to some factors transported by hemodialysis.

Adult↗
PubMedDate not supplied

[Bacterial surface and phagocytosis].

Phagocytosis is a host's front line of cellular defence against bacteria. Some anatomical structures of the bacterial envelope may hinder this cellular activity. Amongst the most important constituents of the cell envelope, the capsule plays a very important role, its biochemical components being polysaccharide (pneumococcus, meningococcus), M proteins (streptococcus, yersinia, E. coli), mucopeptide (staphylococcus) or hyaluronic acid (streptococcus, Treponema pallidum). Complement plays an outstanding role by increasing the phagocytosis index. The studies of the different factors of the complement show that the degree of phagocytosis is correlated with the amount of C3 fixed on the surface of the bacteria. We still do not know the exact nature of the cell receptors, but the surface properties of the host cell and of the bacteria determine the contact angle which is of importance in this process.

Bacteria↗
PubMed1984

Appendix. Structural predictions on alpha 2-macroglobulin from the amino acid sequence.

The composite result from three different methods predicts that alpha 2-macroglobulin has a predominant pattern of alternating beta-strands and turns. Only scattered pieces of alpha-helix are present throughout its sequence. Predicted beta-strands constitute 43.8% and helices 8.6%, in fair agreement with circular dichroism spectra. Circular dichroism spectra and sequence data suggest that the tertiary structure of complement component C3b is similar to that of the alpha 2 macroglobulin monomer. At present, the beta-barrel configuration of prealbumin seems to be a better model than those of soybean trypsin inhibitor, serine proteases, and immunoglobulins. A repetitive pattern of disulfide loops could indicate structural units of about 200 residues in size, but this is not supported by amino acid sequence homology. The hydropathic pattern of the sequence reveals numerous examples of predicted immunogenic peptides and detects an approximately 100-residue hydrophobic core region, which could constitute parts of the tentatively assigned consecutive activation cleavage and thiol ester domains. This core is an obvious candidate of rearrangement transfer between the highly exposed bait region and the partly shielded thiol ester site. The presumed intersubunit half-cystine is moderately buried and has two nearby patches of high charge density which could guide the dimeric assembling.

Amino Acid Sequence↗
PubMed1980

B cell markers in Ph1-positive acute lymphoblastic leukemia.

A case of acute lymphoblastic leukemia (ALL) where the blast cells had B cell markers and displayed the presence of a typical Ph1 chromosome, originated by a standard t (9;22) translocation, is reported. Cytological and clinical aspects during the entire course of the disease were consistent with the diagnosis of ALL. Evidence of differentiation along a well-defined lymphoid cell line in a Ph1-positive cell confirms the presence of the Ph1 chromosome in conditions other than chronic granulocytic leukemia and shows that it possibly does not occur in an exclusively undifferentiated totipotent stem cell.

Adult↗
PubMed1994

Mechanism of antigenic variation in Shigella flexneri. II. Sensitivity to complement as a selection factor for antigenic mutant 3b in 1b serotype.

In the first report we stated that the antigenic mutant of Shigella flexneri 6713 3b serovar with antigenic formula III: 3, 4, 6 was less sensitive to bactericidal action of normal calf serum in comparison to its parent strain S. flexneri 6713 1b with antigenic formula III: 3, 4, 6. In this paper we show that the phenomenon is rather a general one; the difference in sensitivity was observed in three other strains S. flexneri 1b of independent clinical origin and its antigenic mutants 3b respectively. As the result of serial treatment of these strain with the serum among the survivors the antigenic mutants have been found. In the artificial mixtures of the mutants and isogenic original strains treated with the serum the later show clear cut higher survival.

Antigenic Variation↗
PubMed1994

A low molecular weight phagocytosis-inhibitory factor obtained from human erythrocyte membranes specifically down-regulates Mac-1 activity on tetradecanoyl phorbol acetate-stimulated monocytic cell lines in a Ca(2+)-dependent manner.

A low molecular mass (< 3 kDa) phagocytosis-inhibitory factor (PIF), was partially purified from human erythrocyte membranes. PIF inhibits latex phagocytosis and C, as well as FcR-mediated phagocytosis, by macrophage-like cells in a Ca(2+)-dependent manner. This phagocytosis-inhibitory activity is reversible because removal of PIF restores phagocytic capability of cells. After treatment with PIF, Mac-1 Ag (CR3 or CD11b) becomes almost undetectable on the cell surface by immunofluorescence staining using the mAbs D-12 and BEAR-1, whereas staining with the LM2/1 anti-Mac-1 mAb proved that Mac-1 is still present on the cell surface, thus, indicating a possible conformational change in Mac-1. PIF has no significant inhibitory effect on staining of CR1 (CD35), CR2, (CD21), 20-kDa homologous restriction factor (CD59), decay-accelerating factor (CD55), LFA-1 (CD11a), or p150.95 (CD11c). Although binding of Mac-1-bearing U-937 cells to C3bi-opsonized beads is completely blocked, binding via Con A and FcRs remains unaffected by PIF treatment. In addition to the suppressive effect on phagocytosis, inhibition of cell adhesion was observed as well. The inhibitory effect of PIF on cell adhesion is not monocyte specific, because after exposure to PIF the TGW neuroblastoma cell line lost its ability to attach to the tissue culture plate, but retained its ability for homotypic aggregation. The possibility that PIF is a natural regulator of erythrophagocytosis is suggested.

Blood Proteins↗
PubMed1993

Ligand specificity of purified complement receptor type three (CD11b/CD18, alpha m beta 2, Mac-1). Indirect effects of an Arg-Gly-Asp (RGD) sequence.

We have purified CR3 to homogeneity by affinity chromatography on C3bi-Sepharose and elution with EDTA. C3bi-coated erythrocytes bound to this purified CR3, and binding was dependent on the concentration of both C3bi and CR3, as well as on temperature and the presence of divalent cations. Moreover, binding could be blocked by mAb against CR3 or C3bi and could be enhanced by the addition of integrin modulating factor-1. We used the purified CR3 to test whether several putative ligands of CR3 directly bound the receptor. The interaction of purified CR3 with fibrinogen, filamentous hemagglutinin of Bordetella pertussis, lipophosphoglycan and glycoprotein 63 of Leishmania mexicana, and lipopolysaccharide from Escherichia coli was confirmed. However the interaction of CR3 with zymosan or its major component, beta-glucan, was not observed in these assays. Previous studies showed that binding of C3bi to PMN could be blocked with Arg-Gly-Asp (RGD) containing peptides and were interpreted to indicate that the RGD sequence in C3bi interacts directly with CR3. We found, however, that RGD containing peptides were unable to block the interaction of C3bi with purified CR3, yet retained the ability to block binding of C3bi to cells. We conclude that RGD-peptides do not directly bind CR3, but instead indirectly effect CR3 function. Inasmuch as the effect of RGD-peptides could be mimicked with antibodies against leukocyte response integrin, we suggest that RGD-peptides may bind to leukocyte response integrin on polymorphonuclear leukocytes and influence CR3 activity via this receptor.

Amino Acid Sequence↗
PubMedDate not supplied

[Comparison of the effects of isoflurane and alfentanyl on the mononuclear-phagocytic system].

BACKGROUND AIMS: The effects of two anesthetic agents, alfentanil and isoflurane, on the macrophage-monocytic system and the relation with the adrenocortical-hypophyseal axis were analyzed. MATERIAL AND METHODS: Thirty ASA I-II patients submitted to elective surgery were distributed into two groups: group I, analgesic anesthesia with alfentanil 100 micrograms/kg, a perfusion of 2-3 micrograms/kg/min and naloxone 0.2-0.4 mg upon termination of surgery; group II, inhalation anesthesia with isoflurane at 2-2.5% and O2/air = 1/1. HLA-DR membrane receptors and vimentin threads of the cytoskeleton were determined in basal conditions, at one hour and two hours of induction and upon termination of surgery by means of indirect immunofluorescence with the use of monoclonal antibodies. Phagocytosis of latex particles was also measured and ACTH and cortisol levels were obtained by radioimmunoassay. RESULTS: In group I (alfentanil) a decrease (p < 0.01) of all the monocyte parameters analyzed, which was more significant than that observed in group II (isoflurane), was observed. In group II only the expression of HLA-DR and the index of phagocytosis (p < 0.05) were statistically significant. Following the administration of naloxone a reversion of these parameters was observed. The maximum immune depression corresponded with the lowest values of ACTH and cortisol (group I) with surgical stress being discarded as the cause of this immunodepression. CONCLUSIONS: Alfentanil produces a monocytic depression which reverses following the administration of naloxone, thus discarding surgical stress as the cause of this immunodepression suggesting a mechanism mediated by opiate receptors. With regards to isoflurane, the functions of the mononuclear-phagocytic system were hardly altered in the patient studied.

Adrenocorticotropic Hormone↗
PubMed1996

Activation of human monocyte functions by tumor necrosis factor: rapid priming for enhanced release of superoxide and erythrophagocytosis, but no direct triggering of superoxide release.

Tumor necrosis factor (TNF), like granulocyte-macrophage colony-stimul ating factor (GM-CSF), rapidly primed human monocytes for enhanced release of superoxide (O-2) stimulated by receptor-mediated agonists, N-formyl-methionyl-leucyl-phenylalanine (FMLP) and concanavalin A (Con A), but not by phorbol myristate acetate (PMA), which bypasses the receptors to stimulate the cells. The optimal priming was obtained by pretreatment of suspended monocytes with 10 U/mL TNF for 10 minutes at 37 degrees C. The potency of the maximal priming effect was TNF> GM-CSF, and the combined effect of TNF and GM-CSF was greater than that of each cytokine alone. GM-CSF induced an increase in cytoplasmic pH but TNF did not. These findings suggest that TNF and GM-CSF activate monocytes through different mechanisms. TNF and GM-CSF by themselves never triggered O-2 release in suspended monocytes or monocytes adherent to endothelial cells, although both cytokines triggered massive release of O-2 in human neutrophils. In additions, TNF and GM-CSF induced tyrosine phosphorylation of a 42-kD protein in neutrophils but not in monocytes. These findings suggest that the TNF-receptor- or GM-CSF-receptor-mediated signaling pathways for triggering O-(2) release is active in neutrophils but inactive or defective in monocytes. TNF also enhanced phagocytosis of sialidase-treated autologous erythrocytes by monocytes, and this effect was further potentiated in the presence of autologous fresh serum. The significant enhancement of erythrophagocytosis was obtained at 1 U/mL TNF. At this concentration of TNF, the expression of C3bi-receptor (CD11b/CD18) was upregulated. These findings show that TNF rapidly primes human monocytes for enhanced release of O-(2) and erythrophagocytosis and suggest that TNF activates monocytes through autocrine or paracrine mechanisms at the inflammatory sites inasmuch as TNF is primarily produced by activated monocytes/macrophages.

Adult↗
PubMed1996

Molecular characterization of antigenic polymorphisms (Ond(a) and Mart(a)) of the beta 2 family recognized by human leukocyte alloantisera.

We show that the previously described alloantisera Ond and Mart, which recognize the alloantigens Ond(a) and Mart(a), react with polymorphic variants of alpha L and alpha M subunits of the beta 2 integrin family (CD11a and CD11b molecules). This was shown by testing the alloantisera in a monoclonal antibody-specific immobilization of leukocyte antigens, immunoprecipitation, and immunofluorescence assay against cells from normal donors and from patients with leukocyte adhesion deficiency (beta 2 intergrin deficient). To elucidate the molecular basis of the Ond(a) and Mart(a) alloantigens, RNA was isolated from mononuclear leukocytes derived from individuals of known serologic phenotype. Reverse transcriptase-polymerase chain reaction (RT-PCR) was performed to amplify the entire coding region of the alpha L and alpha M mRNAs. The Ond(a) antigen was found to be due to a G2466C substitution in the DNA coding for the alpha L subunit, which predicts an Arg766Thr amino-acid polymorphism. The Mart(a) antigen was also found to be due to a single nucleotide substitution (G302A) in the DNA coding for the alpha M subunit, which predicts an Arg61His amino acid polymorphism. Using allele-specific restriction enzyme analysis, the association between point mutations and phenotypes was confirmed. The localization of these alloantigens on integrin molecules further illustrates the polymorphic nature of this class of proteins. Whether the polymorphisms influence the adhesive capacity of the leukocyte integrins remains to be investigated.

Alleles↗
PubMed1998

Role of the hypervariable region in streptococcal M proteins: binding of a human complement inhibitor.

Antigenic variation allows pathogenic microorganisms to evade the immune system of the infected host. The variable structure must play an important role in pathogenesis, but its function is in most cases unknown. Here, we identify a function for the surface-exposed hypervariable region of streptococcal M5 protein, a virulence factor that inhibits phagocytosis. The hypervariable region of M5 was found to bind the human complement inhibitor FHL-1 (factor H-like protein 1), a 42-kDa plasma protein. Plasma absorption experiments with M5-expressing bacteria showed that the interaction with FHL-1 occurs also under physiologic conditions. Studies of another extensively characterized M protein, M6, indicated that this protein also has a binding site for FHL-1 in the hypervariable region. The complement-inhibitory function of FHL-1 was retained after binding to streptococci, suggesting that bound FHL-1 protects bacteria against complement attack. All available data now indicate that FHL-1, or another human complement inhibitor, binds to the hypervariable region of M proteins. These findings provide insights into the forces that drive antigenic variation and may explain why the hypervariable region of M protein is essential for phagocytosis resistance. Moreover, these data add to a growing body of evidence that human complement inhibitors are major targets for pathogenic microorganisms.

Antigenic Variation↗
PubMed1998

Monocyte induction of IL-10 and down-regulation of IL-12 by iC3b deposited in ultraviolet-exposed human skin.

CD11b+ monocytic/macrophagic cells (Mo/Mph), which infiltrate into skin after UV irradiation, play an important role in UV-induced immunosuppression. Because in mice, blockade of CD11b (iC3b receptor) on monocytes and depletion of its ligand, iC3b, reverses UV-induced immunosuppression, we asked whether iC3b is deposited in human skin after UV, and whether iC3b can modulate the cytokine profile of Mo/Mph. Immunofluorescence studies revealed that iC3b was newly deposited in UV-exposed skin and was localized in apposition to infiltrating CD11b+ Mo/Mph. In addition, in situ hybridization studies showed that TNF-alpha mRNA was also induced in a similar microanatomic localization. To model the effects of these complex signals on infiltrating Mo/Mph following UV exposure, we then tested the effects of immobilized iC3b and TNF-alpha on resting blood monocytes. Both IL-10 mRNA synthesis and protein secretion were significantly induced by binding of iC3b in vitro and were synergistically increased by the presence of TNF-alpha. The effect was abrogated by a blocking Ab to CD11b, indicating CD11b-iC3b interaction. In contrast, iC3b binding resulted in suppression of IL-12 p40 mRNA and significantly inhibited the production of IL-12 p70 protein. Our studies thus define a novel mechanism for induction of tissue Mo/Mph into an IL-10high/IL-12low state via iC3b in combination with TNF-alpha.

Adult↗